Evidence map›Paper›PMID 29189991›Full record

ArticleDigestive diseases and sciences2018

CSN5 Promotes Hepatocellular Carcinoma Progression by SCARA5 Inhibition Through Suppressing β-Catenin Ubiquitination.

Hongliang Liu, Junwen Hu, Hua Pan, Dilai Luo, Mingwen Huang, Wei Xu

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In one paragraph

Article in Digestive diseases and sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

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  8. Highly ExpressingJournal of immunology research · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Hongliang LiuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China.
Junwen HuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China.
Hua PanDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China.
Dilai LuoDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China.
Mingwen HuangDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China.
Wei XuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No. 1 Min De Road, Nanchang, 330006, Jiangxi Province, China. xuwei19786@126.com.
Second Affiliated Hospital of Nanchang University · CNNanchang University · CN

Funding

Natural Fund Project of Jiangxi Province 20151BAB205086The Project of science and technology support of Jiangxi Provincial 20123BBG70250
6 · The paper itself

Abstract

backgroundIncreasing evidence has suggested that E3 Ubiquitin Ligase CSN5 is a newly characterized oncogene involved in various types of cancer. Scavenger receptor class A member 5 (SCARA5) is an important regulator of biological processes in cancer cells. However, the roles and relationship of CSN5 and SCARA5 in hepatocellular carcinoma (HCC) remain unclear.

methodsWe used RT-PCR, Western blot, and immunohistochemistry to measure CSN5 and SCARA5 expression in HCC tissues and corresponding non-tumor tissues. The CSN5 gene was overexpressed or silenced with lentiviral vectors in HCC cells. Cell proliferation was measured using CCK8 assay. And, the cell migration and invasion were analyzed by transwell assay.

resultsWe found that the expressions of CSN5 and SCARA5 are inversely correlated in HCC tissues, and CSN5 expression levels were negatively correlated with the levels of SCARA5 in various HCC cells. Furthermore, we found that high level of CSN5 expression correlated closely with tumor TNM stage, tumor size, and venous metastasis, but low level of SCARA5 expression correlated closely with tumor TNM stage, tumor size, and venous metastasis. Additionally, survival of patients with lower expression of CNS5 was significantly better than that of higher expression group, but the survival of patients with higher expression of SCARA5 was significantly better than that of lower expression group. Moreover, knockdown of CSN5 increased SCARA5 expression and inhibited the proliferation and metastasis of HCC cells in vitro and in vivo. Finally, we found that CSN5 regulated SCARA5 expression by modulating β-catenin. Mechanistically, our results indicate that CSN5 can decrease β-catenin ubiquitination to enhance the protein expression of SCARA5 in HCC cells.

conclusionsOur data identified CSN5 as a critical oncoprotein involved in progression of HCC cells, which could serve as a potential therapeutic target in HCC patients.

Indexed as

Animalsbeta CateninCarcinoma, HepatocellularCell LineCell ProliferationCOP9 Signalosome ComplexDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLiver NeoplasmsMaleMiceMice, NudeMiddle Agedbeta CateninCOP9 Signalosome ComplexCOPS5 protein, humanIntracellular Signaling Peptides and ProteinsPeptide HydrolasesSCARA5 protein, humanScavenger Receptors, Class ACSN5Hepatocellular carcinomaMetastasisProliferationSCARA5

Identifiers

PMID29189991
OpenAlexW2773053696

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.